Insulin resistance is a physiological condition where the natural hormone insulin becomes less effective at lowering blood sugars. Depending on physical activity and dietary conditions, blood glucose levels may rise outside the normal range and cause adverse health effects. Fat and muscle cells require insulin to absorb glucose. In a dietary state of energy overabundance, cells internally create a cascading process in which insulin receptors on the cell membrane no longer properly interact with insulin. When these cells fail to respond adequately to circulating insulin, glucose is not adequately absorbed, consequently blood glucose levels rise. For many, long periods of insulin resistance precede clinical Type 2 diabetes. During this latent period of insulin resistance blood glucose may be maintained at near normal levels by overcompensation of insulin. It is widely accepted that the diabetic state greatly increases the risk for cardiovascular disease. This process is a continuum and the prediabetic subject also has increased cardiovascular disease risks and inflammation that is primarily associated with insulin resistance.
Convincing evidence has established that insulin resistance is a pre-diabetic state that can predict incident Type 2 diabetes relatively far into the future. Of the diabetic population in the U.S., 90 to 95% suffer from Type 2 diabetes. According to the American Association of Clinical Endocrinologists, up to 80% of Type 2 diabetics are insulin resistant. Numerous studies have documented the development of insulin resistance as a result of increased intake of dietary fats. In both animals and humans, there is an inverse relationship between fasting plasma triglyceride concentration and insulin sensitivity. This medical research associating triglycerides and insulin resistance has practical applications. A multifaceted diabetic medical nutrition therapy program that simultaneously addresses lipids, triglycerides, and insulin resistance can greatly increase the efficacy of a diabetic management program. Recent clinical studies have shown excellent sensitivity at measuring insulin resistance with a triglyceride/glucose index. Others have observed the connections between oxidative stress indicators and lower antioxidant levels.
Elevated Body Mass Index (BMI) is well associated with and the primary contributor to insulin resistance but the initial events triggering the development of insulin resistance and its causal relations with deregulation of glucose and fatty acids metabolism remain unclear. There is clear evidence that insulin resistance is associated with increased oxidative stress and that oxidative stress is the causal agent for insulin resistance. Oxidative stress also disrupts internal antioxidant mechanisms.
Numerous studies have linked increased oxidative stress to insulin resistance. In diabetics, oxidative stress increased and antioxidant defenses are diminished. In both normal individuals and Type 2 diabetic patients, reduction of oxidative stress improved insulin sensitivity as well as improved Beta-cell function. Most Type 2 diabetics are significantly influenced by insulin resistance. A number of researchers have demonstrated that the activities of pathways for reactive oxygen species (ROS) production and oxidative stress increase in liver, muscle and fat tissue in animals and humans before the onset of insulin resistance. Reducing insulin resistance also offers a protective effect on beta-cells. This is very important for the long-term preservation of insulin secretion. Clinical trials have demonstrated improvement of insulin sensitivity in insulin resistance and diabetic patients treated with antioxidants.
Recent landmark research from M.I.T. and the Harvard Medical School indicates that increased oxidative stress levels are an important trigger and causal agent for insulin resistance in numerous physiological settings and that antioxidants were able to decrease insulin resistance caused by oxidative stress. Other researchers have also found that glycemic control and oxidative stress are seen to be tightly related, and improving glycemic control is associated with a lowering of oxidative stress. Reducing oxidative stress can also improve glycemic control. Antioxidants have been shown to reduce oxidative stress and in turn improve insulin secretion and decrease insulin resistance in diabetics. Accordingly, medical nutrition therapy for humans concerned with diabetes should include decreasing fatty acids and increasing intake of effective antioxidants.
Antioxidants should be administered in an effective manner. Many antioxidants work only in specific chemical reactions within the body. Thus, single antioxidant dosages may overload the body with one antioxidant, and saturate that one chemical reaction, but not address the more complex and holistic oxidative stress problem. Some oxidative stress occurs within the cell with over-production of mitochondrial NADH. Many antioxidants are not able to provide intracellular relief of oxidative stress. Antioxidants have demonstrated the ability to decrease oxidative stress, thus preserving Beta-cell function, increasing insulin sensitivity, protecting vascular cell integrity, and repairing nerves in diabetes damaged organs. Additionally, oxidative stress has been documented to inversely affect mitochondrial activity and oxidative stress has been found to be a relevant negative regulator of insulin secretion. Because of the negative effects of oxidative stress, nutrition experts suggest that daily intake should be at least 3,000 to 5,000 Oxygen Radical Absorbance Capacity (“ORAC”) units to have a significant impact on plasma and tissue antioxidant capacity. According to estimates however, the average American consumes only 1,000 to 2,000 ORAC units per day. What is needed therefore is a nutritional supplement that makes up for this deficiency in daily antioxidant intake of ORAC units.